Low-grade alimentary lymphoma (LGAL) was diagnosed by histological and immunohistochemical evaluation of full-thickness biopsies from multiple regions of the gastrointestinal tract collected during exploratory laparotomy in 17 cats. The most common clinical signs were weight loss (n=17) and vomiting and/or diarrhoea (n=15). Clinical signs were chronic in 11 cases. Abdominal palpation was abnormal in 12 cats, including diffuse intestinal thickening (n=8), an abdominal mass due to mesenteric lymph node enlargement (n=5) and a focal mural intestinal mass (n=1). The most common ultrasonographic finding was normal or increased intestinal wall thickness with preservation of layering. Ultrasound-guided fine-needle aspirates of mesenteric lymph nodes (n=9) were incorrectly identified as benign lymphoid hyperplasia in eight cats, in which the histological diagnosis from biopsies was lymphoma. There was neoplastic infiltration of more than one anatomic region of the gastrointestinal tract in 16/17 cats. The jejunum (15/15 cats) and ileum (13/14 cats), followed by the duodenum (10/12 cats), were the most frequently affected sites. Twelve cats were treated with oral prednisolone and high-dose pulse chlorambucil, two with a modified Madison-Wisconsin multiagent protocol and three with a combination of both protocols. Thirteen of the 17 cats (76%) had complete clinical remission with a median remission time of 18.9 months. Cats that achieved complete remission had significantly longer median survival times (19.3 months) than cats that did not achieve complete remission (n=4) (4.1 months; P=0.019). The prognosis for cats with LGAL treated with oral prednisolone in combination with high-dose pulse chlorambucil is good to excellent.

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Medical records (2005-2009) of a feline-only practice were searched for cats with degenerative joint disease (DJD) treated using meloxicam. DJD was diagnosed by the presence of at least two of the following: (i) altered mobility (observed by the owner), (ii) abnormal physical findings, (iii) characteristic radiographic changes. The primary study cohort consisted of cats older than 7 years that had received meloxicam for variable intervals in excess of 6 months, and for which complete records were available. These cats were subdivided according to whether detectable chronic kidney disease (CKD) was present ('renal group'), or not ('non-renal group'), and, for the 'renal group', according to the cat's IRIS category. Serum biochemistry, urinalysis (including urine specific gravity [USG]), body mass and condition score were monitored regularly. Progression of CKD in the 'renal group' and 'non-renal group' of cats was compared to two groups of age- and IRIS-matched control cats not receiving meloxicam (from the same clinic, over the same time period). The study was thus a case-control design, with two study groups. Thirty-eight cats with DJD receiving long-term meloxicam therapy met the inclusion criteria. Of these, 22 cats had stable CKD at the start of treatment (stage 1, eight cats; stage 2, 13 cats; stage 3, one cat). No cats initially had an elevated urinary protein to creatinine ratio. The remaining 16 cats initially had normal renal analytes and adequately concentrated urine. The median age of the 'renal' and 'non-renal' meloxicam groups was 15.5 and 13.4 years, respectively. The median treatment duration was 467 days in the 'renal group' and 327 days in the 'non-renal group'. After titration (to the lowest effective dose), the median maintenance dose was 0.02 mg/kg/day in both groups (range 0.015-0.033 mg/kg/day). There was no difference in sequential serum creatinine concentration or USG measurements between the 'non-renal group' treated with meloxicam compared to control cats not treated with meloxicam. There was less progression of renal disease in the 'renal group' treated with meloxicam compared to the age- and IRIS-matched cats with CKD not given meloxicam. These results suggest that a long-term maintenance dose of 0.02 mg/kg of meloxicam can be safely administered to cats older than 7 years even if they have CKD, provided their overall clinical status is stable. Long-term meloxicam therapy may slow the progression of renal disease in some cats suffering from both CKD and DJD. Prospective studies are required to confirm these findings.

This is the first Australian study to determine the prevalence of R. felis and B. clarridgeiae in both fleas and the cats from which they were collected. Flea-associated infectious agents are common in cats and fleas in eastern Australia and support the recommendation that stringent flea control be maintained on cats.

The study sought to examine the effect of long-term meloxicam treatment on the survival of cats with and without naturally-occurring chronic kidney disease at the initiation of therapy. The databases of two feline-only clinics were searched for cats older than 7 years that had been treated continuously with meloxicam for a period of longer than 6 months. Only cats with complete medical records available for review were recruited into the study.The median longevity in the renal group was 18.6 years [95% confidence interval (CI) 17.5-19.2] and the non-renal group was 22 years [95% CI 18.5-23.8]. The median longevity after diagnosis of CKD was 1608 days [95% confidence interval 1344-1919] which compares favourably to previously published survival times of cats with CKD. In both groups the most common cause of death was neoplasia. Long-term treatment with oral meloxicam did not appear to reduce the lifespan of cats with pre-existent stable CKD, even for cats in IRIS stages II and III. Therefore, to address the need for both quality of life and longevity in cats with chronic painful conditions, meloxicam should be considered as a part of the therapeutic regimen.

A total of 38 cases of naturally occurring intestinal tritrichomoniasis in Australian cats are described. Detailed information was available for 13 cases diagnosed in two veterinary hospitals, one in Victoria and one in New South Wales (NSW). In all instances, presumptive microscopic diagnoses were confirmed by polymerase chain reaction (PCR) testing. Affected cats were generally young (median age 8 months) and of a pedigree breed (12/13 cats; 92%). Diarrhoea was observed in 10 cats (77%); the remaining three cats were asymptomatic and detected by screening undertaken because these cats cohabited with symptomatic cases. Concurrent infections with Giardia species (7/13 cats; 54%), and Toxocara species and Eucoleus species (2/13 cats; 15%) were identified. Treatment of tritrichomoniasis with ronidazole at a dose of 30mg/kg once or twice a day, in concert with appropriate therapy of concurrent gastrointestinal infections, resolved diarrhoea in all cats treated. Limited case details of a further 25 infected cats were obtained from a commercial laboratory offering a real-time PCR assay for Tritrichomonas foetus, and compared with findings from the 13 cats presenting to the contributing veterinary hospitals. All samples submitted to this laboratory returning a positive PCR result were from pedigree cats maintained in multi-cat facilities. Most of the samples were derived from Victoria (4/8 catteries tested; 50%), although positive samples were also identified from cats in NSW (1/4 catteries tested; 25%), Queensland (1/4 catteries; 25%), Tasmania (1/4 catteries; 25%) and South Australia (1/4 catteries; 25%). Our impression is that intestinal tritrichomoniasis is an emerging infectious disease of Australian cats. Tests to detect T foetus should be a routine component of the work-up of chronic diarrhoea in cats, especially young purebred cats.

Low-grade alimentary lymphoma (LGAL) requires histological assessment of biopsies for diagnosis whereas intermediate- (IGAL) and high-grade (HGAL) alimentary lymphoma (AL) can be diagnosed by cytology of intestinal or mesenteric lymph node aspirates. Assessment of the relative frequency of subtypes of AL using histology alone may be skewed towards an increased frequency of LGAL as cases of IGAL or HGAL diagnosed cytologically may not progress to biopsy. We investigated the relative prevalence of AL subtypes diagnosed by both histopathology and cytology among primary accession cases across Australia during a 5-year period. Clinicopathological features of LGAL were compared with those of IGAL/HGAL. Fifty-three cases of AL were identified, including 30 diagnosed by histology (15 LGAL, 13 HGAL, two IGAL) and 23 IGAL/HGAL diagnosed by cytology. LGAL cases comprised 50% of histological diagnoses, but only 28% of all AL. A palpable abdominal mass was more common in IGAL/HGAL (43%) than in LGAL (7%) [odds ratio (OR) 7.6, P = 0.01]. Anaemia was more common in IGAL/HGAL (41%) compared with LGAL (7%) (OR 9.6, P = 0.02). On abdominal ultrasound, a gastrointestinal mural mass was visualised in 41% of IGAL/HGAL and 0% of LGAL (P = 0.01). Where a detailed abdominal ultrasound report was provided, gastric/intestinal wall thickening was the most commonly reported abnormality (82%). In cats with intestinal thickening, a loss of normal layering was more common (P = 0.02) in cats with IGAL/HGAL (71%) compared with those with LGAL (20%). The relative prevalence of LGAL was lower when cases diagnosed by cytology were included in addition to those diagnosed by histology in the study population. The relative frequency with which LGAL is diagnosed has increased since initial reports from this region. A number of significant clinicopathological findings are useful to distinguish LGAL from IGAL/HGAL.

Objective-To determine the frequency of the mutant pyruvate kinase (PK) allele, haematological parameters and AB blood types of Abyssinian and Somali cats in Australia.Design-Complete blood cell and reticulocyte counts, DNA PK mutation testing and blood typing were performed in all cats.Results-A total of 60 cats (36 Abyssinians, 24 Somalis) were included (37 females, 23 males). For the mutant PK allele, three female Somalis were homozygous (affected, 5%), 17 cats were heterozygous (carrier, 28%) and 40 cats tested negative (normal, 67%). Pedigree analysis revealed common ancestry of affected and many carrier cats. Of affected cats, two had regenerative anaemias and all had reticulocytosis (range 64-390 × 10 9 /L; P < 0.001 compared with normal or carrier cats). The only consistent historical sign was lethargy. One affected cat was euthanased 18 months after testing, because of anaemia, neutropenia, anorexia and weight loss. The mutant allele frequency was 0.19 overall (0.29 in Somalis, 0.13 in Abyssinians). All cats had blood type A. The commercial blood typing card method incorrectly identified 12 cats as having type AB blood.Conclusions-The frequency of the mutant PK allele is high in Australia. Screening for PK deficiency is indicated before mating and in individual cats of these breeds, even in the absence of anaemia and especially when there is reticulocytosis. Although all cats in the present study had blood type A, blood type B is common in these breeds worldwide. Retyping of any AB typed cats by a laboratory technique is recommended. Keywordscats; blood type; congenital; red blood cell abnormality; feline; haemolytic anaemia; neonatal isoerythrolysis; pyruvate kinase Pyruvate kinase (PK) deficiency, a glycolytic erythroenzymopathy, was first documented in humans in the early 1960s, 1 in basenji and beagle dogs in the 1970s 2,3 and in Abyssinian and Somali cats in the early 1990s. 4,5 Because erythrocytes lack mitochondria, they rely on anaerobic glycolysis for energy production. PK catalyses one of the two major steps of ATP production in red blood cells (RBC) through conversion of phosphoenolpyruvate to pyruvate. ATP is essential for RBC functions, including maintenance of shape and deformability, membrane transport and metabolic functions. PK deficiency thus results in ATP depletion, with reduced erythrocyte survival and haemolytic anaemia. 6-9 NIH Public Access Materials and methodsCats were recruited into the study from the Abyssinian Cat Club of Australasia. Approval for this study was granted by The University of Sydney Animal Care and Ethics Committee. Any cat was eligible unless it or both its parents had been previously tested for PK deficiency. All cats were scanned for the presence of a microchip and pedigrees (required minimum of four generations) were matched with the microchips. After physical examination, 1.5 to 2 mL of blood was collected by jugular venipuncture into EDTA tubes. Sampling was carried out at the Valentine Charlton Cat Centre, University of Sydney, New South Wales,...